Clinical techniques for assessment of fetal health and neurological development are inadequate. In large part, this is due to the limitations and difficulties of conducting and interpreting human studies without recourse to appropriate model systems. Research with the baboon (papio sp.) has demonstrated many homologies between this species and humans, particularly with respect to fetal physiological, endocrine, and neurobehavioral function. These homologies include th predominant features of fetal behavioral state and of state dependent cardiovascular and breathing activity. in addition, key aspects of placental morphology and function including hormone production and nutrient transport, of integrated maternal and fetal pituitary-adrenal activity, and factors which reflect cellular reactivity to hypoxemia/hypoxia are common to both baboons and hum s. Our aims are to refine methods for inducing varying durations and degrees of fetal oxygen deprivation, and then to characterize athe changes in breathing activity, heart rate, and behavioral stat e as the fetus adapts to hypoxic challenges. The overall objective is to distinguish between normal variation and adaptive alterations in the organization of fetal physiology and behavior. These aims will be accomplished using methods in which baboon mothers and their fetuses are instrumented and chronically monitored during the last third of gestation. The technology for these studies, which was developed under the auspices of this Center, is unique in that information from multiple maternal and fetal sensors is recorded continuously from the unanesthetized unrestrained pregnant baboon in her home cage. The system also permits sampling from, and infusion into, maternal and fetal blood and amniotic fluid. In addition to these aims, this project is central to the PERC because it provides a model for non-human primate research to be used by the Center's Investigators. In these collaborative aims, a number of other important questions concerning the adaptive responses of the fetus to oxygen and nutrient deprivation will be addressed: Does acute fetal hypoxia activate the endothelium and foster procoagulation? What are the roles of cortisol, sex steroids, and cytokines in the mechanisms regulating placental CRH: What are the patterns of the pro-opiomelanocortin peptides and steroid hormones released by stimulation of the fetal pituitary-adrenal axis by acute hypoxia, and is the pattern different with chronic oxygen deprivation? Does placental CRH modulate athe effects of chronic hypoxia on fetal adrenal and placental endocrine function? Together, these experiments will provide key information about fetal physiology, and adaptations and responses to oxygen deprivation that are unique to tahe primate but not available from human investigation.